Matches in SemOpenAlex for { <https://semopenalex.org/work/W1487201207> ?p ?o ?g. }
Showing items 1 to 92 of
92
with 100 items per page.
- W1487201207 abstract "Defects in myocardial energy metabolism have been linked to pathological cardiac hypertrophy and congestive heart failure; however, the regulation of myocardial energy metabolism remains obscure. ATP synthase is an enzyme complex in the mitochondria and plays a central role in energy metabolism. In the present study, we identified ES1, a mitochondrial protein with unknown function, as a key determinant of myocardial energy metabolism via controlling ATP synthase activities. We uncovered that ES1 interacts with both α and β subunit of ATP synthase, and its expression levels in cultured H9c2 cardiomyocytes were directly correlated to ATP synthesis and inversely to ATP hydrolysis. Cellular energetic analysis revealed that ES1 levels in H9c2 cardiomyocytes were directly correlated with mitochondrial oxidative metabolism. We have generated an ES1 knockout mouse (ES1-/-) line. Echocardiography revealed substantially cardiac dysfunction with decreased ejection fraction (EF%) (55.3 ± 2.4 vs 46.1 ± 1.7) and fractional shortening (FS%) (28.6 ± 1.6 vs 22.8 ± 1.0) in 3-month-old ES1-/- mice compared with controlled littermates (ES1f/f) under a basal condition. As a result, ES1-/- mice showed increased left ventricular mass compared. Morphometric assessment confirmed that heart weight to body weight ratio was increased by 23% in ES1-/- vs controlled mice. Masson’s Trichrome blue and Sirius red staining on heart sections of ES1-/- mice showed markedly increased interstitial fibrosis. Transmission electron microscope (TEM) examination revealed substantial loss of mitochondrial cristae structure on ES1-/- knockout hearts. ATP synthase activity assays on isolated mitochondria revealed that ATP synthesis activities decreased and hydrolysis activities increased in cardiac mitochondria from ES1-/- mice compared with those of ES1f/f control mice. These results indicate that ES1 is a novel and important ATP synthase regulator and its deficiency causes mitochondrial energy metabolism dysfunction in the heart followed by cardiac pathology. Therefore, ES1 is a important determinant of cardiac pathophysiology and a potential therapeutic target in treating cardiac hypertrophy and heart failure." @default.
- W1487201207 created "2016-06-24" @default.
- W1487201207 creator A5001310235 @default.
- W1487201207 creator A5005880464 @default.
- W1487201207 creator A5011217237 @default.
- W1487201207 creator A5022429262 @default.
- W1487201207 creator A5042196538 @default.
- W1487201207 creator A5068110198 @default.
- W1487201207 creator A5068390739 @default.
- W1487201207 creator A5069033450 @default.
- W1487201207 creator A5071062179 @default.
- W1487201207 creator A5077906192 @default.
- W1487201207 creator A5090635037 @default.
- W1487201207 date "2014-11-25" @default.
- W1487201207 modified "2023-10-06" @default.
- W1487201207 title "Abstract 12456: Mitochondrial Protein ES1 Deficiency Leads to Cardiac Hypertrophy Due to Disturbances in Mitochondrial Energy Metabolism" @default.
- W1487201207 hasPublicationYear "2014" @default.
- W1487201207 type Work @default.
- W1487201207 sameAs 1487201207 @default.
- W1487201207 citedByCount "0" @default.
- W1487201207 crossrefType "journal-article" @default.
- W1487201207 hasAuthorship W1487201207A5001310235 @default.
- W1487201207 hasAuthorship W1487201207A5005880464 @default.
- W1487201207 hasAuthorship W1487201207A5011217237 @default.
- W1487201207 hasAuthorship W1487201207A5022429262 @default.
- W1487201207 hasAuthorship W1487201207A5042196538 @default.
- W1487201207 hasAuthorship W1487201207A5068110198 @default.
- W1487201207 hasAuthorship W1487201207A5068390739 @default.
- W1487201207 hasAuthorship W1487201207A5069033450 @default.
- W1487201207 hasAuthorship W1487201207A5071062179 @default.
- W1487201207 hasAuthorship W1487201207A5077906192 @default.
- W1487201207 hasAuthorship W1487201207A5090635037 @default.
- W1487201207 hasConcept C100206155 @default.
- W1487201207 hasConcept C104317684 @default.
- W1487201207 hasConcept C112243037 @default.
- W1487201207 hasConcept C126322002 @default.
- W1487201207 hasConcept C134018914 @default.
- W1487201207 hasConcept C167414201 @default.
- W1487201207 hasConcept C181199279 @default.
- W1487201207 hasConcept C2778198053 @default.
- W1487201207 hasConcept C28859421 @default.
- W1487201207 hasConcept C2994266630 @default.
- W1487201207 hasConcept C512185932 @default.
- W1487201207 hasConcept C55493867 @default.
- W1487201207 hasConcept C57600042 @default.
- W1487201207 hasConcept C62231903 @default.
- W1487201207 hasConcept C71924100 @default.
- W1487201207 hasConcept C86803240 @default.
- W1487201207 hasConceptScore W1487201207C100206155 @default.
- W1487201207 hasConceptScore W1487201207C104317684 @default.
- W1487201207 hasConceptScore W1487201207C112243037 @default.
- W1487201207 hasConceptScore W1487201207C126322002 @default.
- W1487201207 hasConceptScore W1487201207C134018914 @default.
- W1487201207 hasConceptScore W1487201207C167414201 @default.
- W1487201207 hasConceptScore W1487201207C181199279 @default.
- W1487201207 hasConceptScore W1487201207C2778198053 @default.
- W1487201207 hasConceptScore W1487201207C28859421 @default.
- W1487201207 hasConceptScore W1487201207C2994266630 @default.
- W1487201207 hasConceptScore W1487201207C512185932 @default.
- W1487201207 hasConceptScore W1487201207C55493867 @default.
- W1487201207 hasConceptScore W1487201207C57600042 @default.
- W1487201207 hasConceptScore W1487201207C62231903 @default.
- W1487201207 hasConceptScore W1487201207C71924100 @default.
- W1487201207 hasConceptScore W1487201207C86803240 @default.
- W1487201207 hasLocation W14872012071 @default.
- W1487201207 hasOpenAccess W1487201207 @default.
- W1487201207 hasPrimaryLocation W14872012071 @default.
- W1487201207 hasRelatedWork W1963875941 @default.
- W1487201207 hasRelatedWork W2000643542 @default.
- W1487201207 hasRelatedWork W2008647597 @default.
- W1487201207 hasRelatedWork W2051694207 @default.
- W1487201207 hasRelatedWork W2072431132 @default.
- W1487201207 hasRelatedWork W2083458225 @default.
- W1487201207 hasRelatedWork W2087565549 @default.
- W1487201207 hasRelatedWork W2097049860 @default.
- W1487201207 hasRelatedWork W2141718522 @default.
- W1487201207 hasRelatedWork W2151042012 @default.
- W1487201207 hasRelatedWork W2177819816 @default.
- W1487201207 hasRelatedWork W2190642228 @default.
- W1487201207 hasRelatedWork W219187680 @default.
- W1487201207 hasRelatedWork W2218281936 @default.
- W1487201207 hasRelatedWork W2233583597 @default.
- W1487201207 hasRelatedWork W2612931260 @default.
- W1487201207 hasRelatedWork W2729856087 @default.
- W1487201207 hasRelatedWork W2889393736 @default.
- W1487201207 hasRelatedWork W2921719364 @default.
- W1487201207 hasRelatedWork W2946523286 @default.
- W1487201207 hasVolume "130" @default.
- W1487201207 isParatext "false" @default.
- W1487201207 isRetracted "false" @default.
- W1487201207 magId "1487201207" @default.
- W1487201207 workType "article" @default.